Nitric oxide (NO), a multifunctional endogenous gas molecule, is metabolized from L-arginine by enzymatic reaction in the presence of nitric oxide synthase. NO, an important gas signaling molecule, is a gastric mucosa protective factor that contributes significantly to maintain normal gastric mucosa integrity. NO increases gastric mucosa blood flow, regulates the secretion of mucus and bicarbonate, and inhibits the secretion of gastric juice. Asymmetric dimethylarginine (ADMA) has been identified as the major endogenous inhibitor of nitric oxide synthase. The function of ADMA is to decrease NO production via inhibiting nitric oxide synthase activity. Besides inhibiting NO synthesis, ADMA also directly induces oxidative stress and cell apoptosis, and participates in inflammation reaction. Its systemic accumulation was observed in conjunction with several cardiovascular and metabolic diseases. ADMA also mediates gastric ulcer injury induced by ethanol, stress, helicobacter pylori and indomethacin. The mechanism of ADMA directly producing adverse effect in gastric mucosa is incompletely understood. It is widely accepted that NO bioavailability decrease is the majority reason. Promotion of apoptosis and aggravation of inflammation may be other important mechanisms of ADMA-induced gastric injury. ADMA might be a novel clinical and experimental biomarker related to gastric mucosa disorder. Although therapeutic tool targeting to ADMA is available in multiple cardiovascular diseases, it is unknown in gastrointestinal disease. The strategy to inhibit ADMA is beneficial to gastric ulcer induced by ethanol in rats. Thus, ADMA might be a candidate of therapeutic target in gastric mucosa damage.
Keywords: Asymmetric dimethylarginine; Mucosal injury; Nitric oxide.